细胞色素氧化酶mRNA在高氧暴露早产大鼠肺组织中的表达变化

Expression changes of cytochrome oxidase genes in hyperoxia induced lung injury in premature newborn rat.

目的观察85%高浓度氧(高氧)暴露下早产新生大鼠肺组织的病理改变及线粒体DNA编码细胞色素氧化酶亚基(COXI、COXII、COXIII)mRNA表达的动态变化,探讨其在早产大鼠高氧肺损伤发生、发展中的可能作用。方法早产SD大鼠生后1d随机分为空气组、高氧组。高氧组持续暴露于85%氧气中,空气组置于同一室内常压空气中。两组分别于暴露满1、4、7、10和14d时,每组取动物8只,行肺组织病理学检查,半定量逆转录聚合酶链反应测定COXI、COXII和COXIII mRNA的表达。结果(1)高氧暴露4d即可见肺泡炎和肺发育滞后的改变。(2)与同时间点空气组相比,高氧暴露1d和4d时,COXI mRNA的表达显著增强(P<0.05和P<0.01),其后开始下降,7d时两组差异无显著性(P>0.05),10d时较空气组显著降低(P<0.01),14d时复又增高,且明显高于空气组,差异有非常显著性(P<0.01)。COXII和COXIII mRNA在各时间点的表达差异无显著性。结论85%高氧暴露诱导早产新生大鼠肺组织线粒体DNA编码COX亚基异常表达,这种变化可能参与了高氧肺损伤的发生。

Objective To observe the expression of mitochondrial encoding cytochrome oxidase genes （ COXI,COXII,COXIII）in lungs of premature newborn rats exposed to 85 % hyperoxia and explore the role of COX in hyperoxia-induced lung injury. Methods The one-day-old premature SD rats were randomly divided into room air group and hyperoxia group. Hyperoxia group were continuously exposed to 85 % oxygen and air group in room air. After 1,4, 7, 10, 14 days of exposure, eight rats of each group were sacrified to assess lung histopathologic changes. Expression of COXI, COXII and COXIII mRNA were detected by reverse transcrip- tion polymerase chain reaction（RT-PCR）. Results （1） lung pathological changes： On day 4 of exposure, hy- peroxia group showed lung injury characterized by alveolitis and inhibition of lung development. （2） expression of mRNA：As compared with that of room air group, COXI mRNA expression of hyperoxia group first in- creased significantly on day 1 and day 4（ P 〈 0.05 and P 〈 0.01 respectively）, then decreased to the equiva- lent level on day 7（ P 〉 0.05） and a lower level on day 10, but finally recovered the increasing tendency to a significantly higher level on day 14（P 〈 0.01）. There were not significant differences of COXIIand COXIII mRNA expression levels between two groups at every time point. Conclusion Exposure of 85 % hyperoxia has significant impact on the expression of cytochrome oxidase subunits in premature newborn rats, which is likely to contribute to the pathogenesis of hyperoxia-induced lung injury.